Wsv023 interacted with γ-tubulin complex associated proteins 2, and decreased the formation of microtubules.

A previous study found the key transcription factor of PERK-eIF2α pathway cyclic AMP-dependent transcription factor 4 (LvATF4) was involved in the transcriptional regulation of white spot syndrome virus (WSSV) gene . Knocked-down expression of LvATF4 reduced the viral copy number and the cumulative mortality of WSSV-infected shrimp. These results suggested that wsv023 may be critical to WSSV infection but the precise function of wsv023 was still unknown. By using co-immunoprecipitation and pull-down assays, we show that wsv023 interacts with gamma complex-associated protein 2 (LvGCP2), which is the core protein of the γ-tubulin small complex. Knocked-down, the gene significantly reduced the copy number of WSSV in muscle, as well as the cumulative mortality of infected shrimp. And PERK-eIF2α pathway inhibition also showed reduced virus copy number and abrogated shrimp mortality. Furthermore, overexpression of wsv023 inhibited the formation of microtubules in 293T cells. Flow cytometry revealed that WSSV infection similarly decreased the formation of microtubules in haemocytes. These findings suggested that wsv023 plays a role in microtubule organization in host cells, which in turn may be beneficial to WSSV.